The left atrial appendage is a small organ attached to the left atrium of the heart. During normal heart function, as the left atrium constricts and forces blood into the left ventricle, the left atrial appendage constricts and forces blood into the left atrium. The ability of the left atrial appendage to contract assists with improved filling of the left ventricle, thereby playing a role in maintaining cardiac output. However, in patients suffering from atrial fibrillation, the left atrial appendage may not properly contract or empty, causing stagnant blood to pool within its interior, which can lead to the undesirable formation of thrombi within the left atrial appendage. Thrombi forming in the left atrial appendage may break loose from this area and enter the blood stream. Thrombi that migrate through the blood vessels may eventually plug a smaller vessel downstream and thereby contribute to stroke or heart attack. Clinical studies have shown that the majority of blood clots in patients with atrial fibrillation originate in the left atrial appendage. As a treatment, medical devices have been developed which are deployed to close off the ostium of the left atrial appendage. Over time, exposed surface(s) of an implant spanning the ostium of the left atrial appendage may become covered with tissue (a process called endothelization), effectively removing the left atrial appendage from the circulatory system and reducing or eliminating the amount of thrombi which may enter the blood stream from the left atrial appendage.
Unfortunately, the left atrial appendage provides certain positive effects and/or functions, and closing the left atrial appendage off may have some negative side-effects. For example, stretch receptors of the left atrial appendage play a role in mediating thirst in hypovolemia. Effectively eliminating these receptors by closing off the left atrial appendage may cause hypertension and/or may negatively impact systemic blood pressure. Additionally, the left atrial appendage is highly dynamic, and modulates the relationship between pressure and volume, functioning as a natural decompression chamber. Left atrial appendage clamping may lead to an increase in diastolic transmitral and pulmonary flow velocities, and to an increase in left atrial mean pressure and size. Further still, the left atrial appendage is an endocrine organ which releases atrial natriuretic peptide (ANP). Endothelial cells of the left atrial appendage are specialized in the production and release of natriuretic peptides. In healthy human hearts, atrial natriuretic peptide concentration may be several times higher in the left atrial appendage than in the rest of the atrial free wall and in the ventricles. A continuing need exists for improved medical devices and methods to control thrombus formation within the left atrial appendage of patients suffering from atrial fibrillation while accommodating and/or maintaining the positive functionality of the left atrial appendage.